ACUTE INTERSTITIAL NEPHRITIS

Acute interstitial nephritis classically presents with fever, maculopapular rash, eosinophilia, eosinophiluria, and urinary WBC casts.  Eosinophiluria is neither sensitive (sensitivity 40%) nor entirely specific (specificity 72%, positive predictive value 38%).  The classic triad of rash, fever and eosinophilia is actually uncommon and only seen approximately 10% of the time.  One can also see mild proteinuria (usually < 1g/d) and other signs of tubular damage, such as renal tubular acidosis and Fanconi’s syndrome. Renal ultrasound generally reveals kidneys of normal to large size. Gallium scanning has been suggested as an aid to distinguishing this condition from acute tubular necrosis (ATN).  It is negative in ATN but generally positive in interstitial nephritis. 

Drug classes that can cause AIN:

Penicillin analogs (methicillin, ampicillin, etc.)– most common

Cephalosporins

Sulfonamides (sulfamethoxazole,cotrimoxazole)

Other antibiotics such as rifampin andciprofloxacin

NSAIDS (including Cox-2 specific agents)

Diuretics

Proton pump inhibitors

Miscellaneous – this includes a very largenumber of drugs such as allopurinol and cimetidine.

Risks related with renal biopsy

The incidence of gross hematuria is approximately 5-10%

·        The incidence of significant bleeding enough to delay discharge is approximately1:100.  This refers to persistent hematuria, or perinephric hematoma, which usually settles with conservative management

·        A transfusion is occasionally necessary

·        Serious bleeding complications sufficient to warrant interventions to stop bleeding are of the order of 1:1000

·        Kidney biopsy can be life threatening in 1:5000-1:10000 

Nephrolog

Goodpasture’s disease is the most aggressive and rapidly progressive glomerulonephritis
encountered in clinical practice. Crescentic nephritis may be accompanied by lifethreatening
pulmonary hemorrhage.. Treatment with cyclophosphamide, steroids, and plasma exchange can arrest the
disease, but renal damage may be irrecoverabl
. In small-vessel vasculitis, the mainstay of therapy consists of corticosteroids and
cyclophosphamide.. In antineutrophil cytoplasmic autoantibody (ANCA) vasculitis, plasma exchange is
presently recommended in addition to corticosteroids and cyclophosphamide for
patients presenting with advanced renal failure and/or pulmonary hemorrhage.. A high rate of venous thromboembolism has been reported in ANCA vasculitis, with
about 10% of patients developing symptomatic events.